Flores N A, Seghatchian M J, Sheridan D J
Academic Cardiology Unit, St Mary's Hospital Medical School, London, UK.
Blood Coagul Fibrinolysis. 1991 Apr;2(2):367-71. doi: 10.1097/00001721-199104000-00022.
Recent clinical and experimental evidence indicates that platelet activation contributes to the arrhythmogenic effects of myocardial ischaemia, but little is known about the electrophysiological effects produced by controlled platelet activation under conditions of normal perfusion and how these might relate to effects during ischaemia. To investigate this, we studied changes in cardiac cellular electrophysiology and arrhythmogenesis during infusion of platelets [10(8)/ml] in isolated, perfused guinea-pig hearts during normal perfusion and global myocardial ischaemia. Hearts were studied in four groups: group A (n = 4) receiving frozen/thawed (activated) platelets; group B (n = 4) receiving normal platelets in the presence of 10(-9) M platelet activating factor (PAF); group C (n = 9) receiving buffer only during normal perfusion and myocardial ischaemia; group D (n = 9) receiving platelets during normal perfusion and myocardial ischaemia. Infusion of platelets (group D) had no effects during normal perfusion, but activated platelets (group A) decreased action potential duration (APD) from 165 +/- 1 ms to 138 +/- 5 ms (mean +/- SE) at 15 min of normal perfusion (P less than 0.02) and produced ventricular fibrillation (VF) in 3/4 at 21 +/- 1 min. Infusion of platelets in the presence of PAF (group B) produced similar reductions of APD during normal perfusion and VF in 2/4. During ischaemia, platelets (group D) increased the incidence of VF (100% vs 56% group C, P less than 0.05) and enhanced the ischaemia-induced reductions in APD (107 +/- 3 ms vs 121 +/- 5 ms (group C) P less than 0.05 at 15 min).(ABSTRACT TRUNCATED AT 250 WORDS)
近期的临床和实验证据表明，血小板活化会导致心肌缺血的致心律失常作用，但对于在正常灌注条件下可控的血小板活化所产生的电生理效应以及这些效应与缺血期间的效应可能存在何种关联，人们了解甚少。为了对此进行研究，我们在正常灌注和全心肌缺血期间，对离体灌注豚鼠心脏输注血小板[10(8)/ml]时的心脏细胞电生理变化和心律失常发生情况进行了研究。将心脏分为四组进行研究：A组（n = 4）输注冷冻/解冻（活化）血小板；B组（n = 4）在存在10(-9) M血小板活化因子（PAF）的情况下输注正常血小板；C组（n = 9）在正常灌注和心肌缺血期间仅输注缓冲液；D组（n = 9）在正常灌注和心肌缺血期间输注血小板。在正常灌注期间，输注血小板（D组）没有影响，但活化血小板（A组）在正常灌注15分钟时使动作电位时程（APD）从165±1毫秒降至138±5毫秒（平均值±标准误）（P<0.02），并在21±1分钟时使4只中的3只发生室颤（VF）。在PAF存在的情况下输注血小板（B组）在正常灌注期间产生了类似的APD降低，并且4只中的2只发生了VF。在缺血期间，血小板（D组）增加了VF的发生率（100%对C组的56%，P<0.05），并增强了缺血诱导的APD降低（15分钟时为107±3毫秒对C组的121±5毫秒（P<0.05））。（摘要截断于250字）
